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Biomedical subjects

E Heidbreder

Publications and source records attributed to E Heidbreder.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Pharmacokinetics of gadolinium-DTPA in chronic renal insufficiency requiring dialysis].

MRT with gadolinium-DTPA (0.1 mmol/kg body weight) was performed in 10 patients with renal insufficiency requiring dialysis and the clearance of gadolinium-DTPA was studied. After 3 dialysis on 3 successive days more than 97% of the initial concentration of gadolinium-DTPA had been eliminated. Average half-life was 1.87 hours. There were no side effects in any of the patients. Close laboratory observation of liver function showed no significant changes during the period of study. No contra-indication for the use of this contrast medium in patients with renal insufficiency requiring dialysis was found during this study.

Adult↗
PubMed1990

[Regulation of thirst in end-stage kidney insufficiency].

About 30% of hemodialyzed patients are suffering from chronic fluid overload despite advice to restrict the oral fluid intake. To investigate the cause of the abnormal drinking behaviour a clinical study was performed in 51 non-diabetic patients with endstage renal disease exhibiting lower interdialysis weight gain (less than 3 kg, n = 17) and increased interdialysis weight gain (greater than 3 kg, n = 34). Blood pressure, body weight self-estimated thirst intensity before and after hemodialysis were analyzed. Biochemical and behavioral variables were measured including hormonal factors of water and sodium metabolism. Significant differences of dry weight, creatinine, urea nitrogen and thirst intensity were found between the two groups. Catecholamines, renin, angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide exhibited a similar pattern in both groups. Atrial natriuretic peptide decreased during hemodialysis in both groups, angiotensin II, however, and norepinephrine showed an exaggerated response to ultrafiltration rate in polydipsic patients. These results suggest that changes in serum osmolality during hemodialysis did not contribute to thirst and drinking behaviour. It seems that postdialytic hypovolaemia together with higher plasma-angiotensin II-levels is responsible for increased oral intake of fluid and excessive weight gain.

Angiotensin II↗
PubMed1990

Effects of nisoldipine on stress-induced changes in haemodynamics and plasma catecholamines in normotensives and hypertensives.

In a double-blind, placebo-controlled crossover study 10 mg nisoldipine was given orally twice daily for 3.5 days to 12 normotensives and 12 essential hypertensives. In each study period, subjects were exposed to 6 min of physical exercise and 3 min of mental stress following the morning dose on day 3 and 4, respectively. Blood pressure, heart rate, systolic time intervals (day 3 only) and plasma levels of noradrenaline, adrenaline, dopamine as well as dihydroxyphenylglycol (DOPEG; the main presynaptic metabolite of noradrenaline) were determined at rest and at the end of both tests. Nisoldipine increased resting heart rate in normotensives and hypertensives, but reduced resting BP and BP during mental stress in hypertensives only. It also increased plasma concentrations of noradrenaline and DOPEG at rest and plasma noradrenaline concentrations during mental stress in both groups. However, nisoldipine affected neither exercise- nor stress-induced changes in any of the parameters monitored here. There was a correlation between the drug-induced percentage fall in resting BP and the height of BP during placebo treatment. While the resting values of plasma DOPEG were higher in hypertensives than in normotensives, those of plasma noradrenaline were not. Consequently, the linear relationship that existed between the resting plasma concentrations of DOPEG and noradrenaline in both groups was shifted to higher DOPEG levels in hypertensives when compared with normotensives. In conclusion, the effectiveness of nisoldipine in lowering BP was the more pronounced the higher the BP to begin with. Nisoldipine did not attenuate exercise- or stress-induced increases in plasma catecholamines. Essential hypertension may be associated with an enhanced presynaptic formation of DOPEG.

Adult↗
PubMed1990

Impaired response to intrarenal administered atrial natriuretic peptide in ischemic acute renal failure of a transplanted patient.

A 30-year-old male patient suffering from membrano-proliferative glomerulonephritis was transplanted a cadaveric kidney 3 years ago. Five days later the transplant was removed because of fresh thrombosis in larger arteries. Three years after first transplantation a second graft was transplanted. Repeated perfusion scintigraphies of persistent anuric patient showed a delayed perfusion of renal parenchyma, no intrarenal bolus was obtained. Urgently, an arterial angiography was performed. It demonstrated that calibers of renal parenchymal vasculature were narrowed. Suggesting ischemic nature of acute renal failure, 50 micrograms human atrial natriuretic peptide (hANP) was injected intrarenally as bolus. Five minutes after hANP injection in a second angiography a significant improvement of renal blood flow was demonstrated but no amelioration of urine production or electrolyte excretion was observed. Histologically an ischemic lesion of transplant was proven. This finding indicates a blunted excretory response of acute renal failure after kidney transplantation despite of significantly ameliorated renal blood flow visualized radiologically.

Acute Kidney Injury↗
PubMed1990

Atrial natriuretic peptide reverses experimental acute renal failure induced by arginine vasopressin.

Recently, it has been reported that atrial natriuretic peptide (ANP) reverses or prevents acute renal failure induced by norepinephrine in rats. Therefore, we tested the hypothesis that vasoconstrictor doses of arginine vasopressin (VP) can induce renal ischemia and that consequent renal dysfunction is reversed by ANP infusion or bolus injections in rats. Intrarenally infused VP produced a significant decrease of glomerular filtration rate (GFR) and an increase of urinary volume and sodium excretion rate. Systemic blood pressure increased significantly during VP administration. In a second experimental period, ANP was also given intrarenally, control rats received isotonic saline solution. ANP infusion revealed a highly significant increment of GFR, urinary volume and sodium excretion. Blood pressure fell down below values of the preperiod. After cessation of ANP infusion, renal function was reduced again. These results indicate that VP induces a nonoliguric acute renal failure which is reversed by ANP infusion but only at the time of its administration.

Acute Kidney Injury↗
PubMed1990

Angiotensin-converting enzyme inhibition in renal and hypertensive disorders.

Angiotensin-converting enzyme (ACE) inhibitors have been available for about 10 years for the treatment of various forms of hypertension. Essential hypertension responds particularly well to the administration of this group of drugs, especially when combined with diuretics. A pronounced fall in blood pressure can be achieved in renovascular hypertension with high plasma renin levels; when ACE inhibitors were administered in diagnosed renal artery stenosis there was a significant rise in plasma renin activity on the affected side. Renoparenchymatous hypertension and hypertension in diabetes mellitus can also be improved by the long-term administration of ACE inhibitors, and the progression of renal failure in these disorders seems to be slowed down. Side effects such as neutropenia, exanthema, hearing disorders and pronounced hypotension with an acute deterioration in renal function are substance- and dose-dependent; regular monitoring of the patients greatly reduces their occurrence.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

[A fatal course of alcohol-induced ketoacidosis].

Several days after not eating anything while drinking heavily a 45-year-old alcoholic developed severe ketoacidosis. He was admitted to hospital in a stable cardiovascular condition, but already in a comatose state with Kussmaul breathing. There was a marked metabolic acidosis (pH 6.8; base deficit -30 mmol/l), the urine was positive for ketone bodies, and serum lactate was 24 mmol/l. There was a marked hypoglycaemia (40 mg/dl). Despite intensive treatment it was not possible to prevent multiple organ failure, of which the patient soon died.

Acidosis↗
PubMed1988

Assay of catecholamines and dihydroxyphenylethyleneglycol in human plasma and its application in orthostasis and mental stress.

A high performance liquid chromatographic method involving electrochemical detection is described which permits the assay of noradrenaline (NA), adrenaline (A), dopamine (DA), and dihydroxyphenylethyleneglycol (DOPEG) in human plasma and brings about analytical recoveries of 70% and more. This method was used to assess the effects of graded orthostasis and mental stress on the plasma levels of these catechols. Orthostasis elicited increases in plasma NA and DOPEG, but did not cause any change in plasma A and DA. The increases in NA and DOPEG were dependent on the degree of orthostasis and correlated closely (rs = 0.724; n = 30, P less than 0.001). Pretreatment with desipramine abolished the DOPEG response to standing, indicating that orthostasis - induced increases in plasma DOPEG are presynaptic in origin. Mental stress evoked pronounced increases in plasma A, less pronounced increases in plasma NA and no changes in plasma DA and DOPEG. Hence, the simultaneous measurement of plasma NA and DOPEG may help to distinguish between various types of activation of the sympathetic nervous system.

Adult↗
PubMed1988

Reduction of urea generation and muscle protein degradation by adrenalectomy in acutely uremic rats.

The effect of adrenalectomy on the enhanced protein degradation in acute uremia was investigated. Therefore, serum urea nitrogen, urea N appearance and Nt-methylhistidine were followed in bilaterally nephrectomized rats. At 48 h after induction of uremia the animals displayed serum urea nitrogen levels of 223 +/- 9.5 mg/dl as compared to 26.0 +/- 1.0 mg/dl in sham-treated rats. This increment was significantly attenuated in acutely uremic, adrenalectomized animals (176 +/- 6.0 mg/dl). When these rats were substituted with corticosterone (5 mg/kg body weight), serum urea nitrogen readily increased to levels of acutely uremic animals with intact adrenal glands (225 +/- 6.0 mg/dl). The net generation of urea, as determined by the urea N appearance, was significantly increased during acute uremia (370 +/- 26 mg/48 h) as compared to SHAM animals (220 +/- 15 mg/48 h). This increment of urea formation could almost be completely reversed by simultaneous adrenalectomy (238 +/- 20 mg/48 h). When these rats were substituted with corticosterone, the urea N appearance rebounded to values quite comparable to acutely uremic rats with intact adrenal glands (363 +/- 30 mg/48 h). To determine whether skeletal muscle proteins might serve as a source for the enhanced protein degradation in acute uremia, plasma levels of Nt-methylhistidine were measured. Bilaterally nephrectomized rats had Nt-methylhistidine values of 9.6 +/- 1.0 micrograms/ml. In acutely uremic rats without adrenal glands, Nt-methylhistidine levels were found to be significantly decreased (6.0 +/- 0.4 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1988

Atrial natriuretic peptide counteracts angiotensin-II-induced impairment of renal function.

The present study was designed to investigate the effect of atrial natriuretic peptide (ANP) on angiotensin II (AT II)-induced impairment of renal function. Female Sprague Dawley were used in this study. After anesthesia and surgical procedure, animals were infused with AT II at two different doses (group I, 15 micrograms/kg BW/min and group II, 15 ng/kg BW/min) into the left renal artery. Subsequently, alpha-ANP was infused intrarenally (left kidney, LK) at 2 micrograms/kg BW/min. Controls received isotonic saline only. In all cases the right and noninfused kidney (RK) served as control organ. In all animals, AT II led to a dose-dependent compromise of kidney function of the LK. Glomerular filtration rate (GFR) had decreased to 0.16 +/- 0.06 ml/min and 0.41 +/- 0.12 ml/min in group I and II, respectively. Subsequent ANP infusion induced a significant increase of GFR to 0.83 +/- 0.23 (p less than 0.01) and 0.99 +/- 0.20 (p less than 0.05) ml/min in group I and II, respectively. Urinary volume (V) exhibited a slight but not significant increase following AT II infusion. ANP infusion led to a highly significant increase of V in both groups. A less pronounced, but significant increase of absolute sodium excretion of the LK was observed in both groups after AT II infusion. Absolute potassium excretion did not change in this phase of the experiment. ANP infusion induced a significant increase in both parameters. Isotonic saline had no effect on all parameters measured. Mean arterial pressure (MAP) had increased dose dependent following AT II infusion. After ANP infusion, a significant diminution of MAP to basal values was obtained from both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗